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Mitophagy: From Molecular Mechanisms to Diseases
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Mitophagy: From Molecular Mechanisms to Diseases

A special issue of Cells (ISSN 2073-4409). This special issue belongs to the section "Autophagy".

Deadline for manuscript submissions: closed (30 November 2021) | Viewed by 35562

Special Issue Editors

Dr. Nadine Camougrand

E-Mail Website
Guest Editor
Institut de Biochimie et Génétique Cellulaires, CNRS and Bordeaux University, 1 rue Camille Saint Saëns, 33000 Bordeaux, France
Interests: yeast; molecular biology; cell biology; mitochondria; mitochondria metabolism; autophagy; mitophagy
Dr. Ingrid Bhtia-Kissova

E-Mail Website
Guest Editor
Department of Biochemistry, Faculty of Nature Science, Comenius University, Ilkovicova 6, 84315 Bratislava, Slovakia
Interests: yeasts; mitochondria; mitophagy; mitochondrial metabolic disease; aging; apoptosis

Special Issue Information

Dear Colleagues,

As crucial organelles broadly dispersed in most eukaryotic cells, mitochondria are indispensable for various cellular processes, from generating adenosine triphosphate (ATP), synthesizing key metabolites, maintaining calcium homeostasis, and producing endogenous reactive oxygen species (ROS) to regulating necrosis, apoptosis, and autophagy. The process of mitophagy, in which mitochondria are selectively targeted for degradation in autolysosomes or vacuoles, plays a central role in eliminating old or damaged mitochondria, thus maintaining the integrity of the mitochondrial pool. Nonetheless, mitophagy also promotes a reduction of the overall mitochondrial mass as an adaptive response to certain physiological stresses, such as hypoxia, nutrient deprivation, and DNA damage. Therefore, the appropriate regulation of mitochondrial quality, which includes the timely removal of unhealthy mitochondria and the maintenance of steady mitochondrial turnover, is essential for various physiological and pathological processes. Notably, the selective degradation of excess or dysfunctional mitochondria by autophagy has been observed in organisms ranging from yeast to mammals. Defects in mitophagy and the failure to properly modulate mitochondrial turnover in response to various stresses (e.g., energetic and oncogenic stress) have been linked to changes in the mitochondrial metabolism, the production of ROS excess and ferroptosis, heightened inflammasome activation, altered cell fate decisions, and senescence, among other cellular consequences. Mitochondrial dysfunction and defective mitophagy have been widely associated with neurodegenerative diseases. Thanks to the implementation of approaches related to genetics, cell biology, and proteomics, the past two decades have allowed us to begin to understand the mechanisms and regulation of mitophagy, including the roles of ubiquitin‐dependent and receptor‐dependent signals in triggering the mitophagy of damaged mitochondria.

This special issue welcomes original research findings, focused reviews, or shorter perspective articles covering all aspects of mitophagy in different models (yeast, plants, C. elegans, Drosophila, and mammals). We also invite submissions that highlight the current knowledge of molecular mechanisms that regulate mitophagy and provide insight into the role that mitophagy plays in pathophysiological conditions and aging.

Dr. Nadine Camougrand
Dr. Ingrid Bhtia-Kissova
Guest Editors

Manuscript Submission Information

Manuscripts should be submitted online at www.mdpi.com by registering and logging in to this website. Once you are registered, click here to go to the submission form. Manuscripts can be submitted until the deadline. All submissions that pass pre-check are peer-reviewed. Accepted papers will be published continuously in the journal (as soon as accepted) and will be listed together on the special issue website. Research articles, review articles as well as short communications are invited. For planned papers, a title and short abstract (about 100 words) can be sent to the Editorial Office for announcement on this website.

Submitted manuscripts should not have been published previously, nor be under consideration for publication elsewhere (except conference proceedings papers). All manuscripts are thoroughly refereed through a single-blind peer-review process. A guide for authors and other relevant information for submission of manuscripts is available on the Instructions for Authors page. Cells is an international peer-reviewed open access semimonthly journal published by MDPI.

Please visit the Instructions for Authors page before submitting a manuscript. The Article Processing Charge (APC) for publication in this open access journal is 2700 CHF (Swiss Francs). Submitted papers should be well formatted and use good English. Authors may use MDPI's English editing service prior to publication or during author revisions.

Keywords

  • mitochondrial quality control
  • mitochondria turnover
  • mitophagy pathways
  • factors modulating mitophagy
  • molecular signaling towards mitophagy
  • protein-protein interaction and mitophagy
  • mitophaging and mitophagy dysfunction
  • role of mitophagy in metabolic disease
  • contribution of mitophagy to age-related sporadic disorders (such as Parkinson’s disease, Alzheimer’s disease, cardiomyopathies and cancer)
  • mitophagy as a therapeutic target

Published Papers (7 papers)

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Review

14 pages, 9799 KiB  
Review
BAG Family Members as Mitophagy Regulators in Mammals
by Sophie Pattingre and Andrei Turtoi
Cells 2022, 11(4), 681; https://doi.org/10.3390/cells11040681 - 15 Feb 2022
Cited by 10 | Viewed by 2819
Abstract
The BCL-2-associated athanogene (BAG) family is a multifunctional group of co-chaperones that are evolutionarily conserved from yeast to mammals. In addition to their common BAG domain, these proteins contain, in their sequences, many specific domains/motifs required for their various functions in cellular quality [...] Read more.
The BCL-2-associated athanogene (BAG) family is a multifunctional group of co-chaperones that are evolutionarily conserved from yeast to mammals. In addition to their common BAG domain, these proteins contain, in their sequences, many specific domains/motifs required for their various functions in cellular quality control, such as autophagy, apoptosis, and proteasomal degradation of misfolded proteins. The BAG family includes six members (BAG1 to BAG6). Recent studies reported their roles in autophagy and/or mitophagy through interaction with the autophagic machinery (LC3, Beclin 1, P62) or with the PINK1/Parkin signaling pathway. This review describes the mechanisms underlying BAG family member functions in autophagy and mitophagy and the consequences in physiopathology. Full article
(This article belongs to the Special Issue Mitophagy: From Molecular Mechanisms to Diseases)
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15 pages, 1068 KiB  
Review
Mitophagy Regulation Following Myocardial Infarction
by Annie Turkieh, Yara El Masri, Florence Pinet and Emilie Dubois-Deruy
Cells 2022, 11(2), 199; https://doi.org/10.3390/cells11020199 - 07 Jan 2022
Cited by 23 | Viewed by 4382
Abstract
Mitophagy, which mediates the selective elimination of dysfunctional mitochondria, is essential for cardiac homeostasis. Mitophagy is regulated mainly by PTEN-induced putative kinase protein-1 (PINK1)/parkin pathway but also by FUN14 domain-containing 1 (FUNDC1) or Bcl2 interacting protein 3 (BNIP3) and BNIP3-like (BNIP3L/NIX) pathways. Several [...] Read more.
Mitophagy, which mediates the selective elimination of dysfunctional mitochondria, is essential for cardiac homeostasis. Mitophagy is regulated mainly by PTEN-induced putative kinase protein-1 (PINK1)/parkin pathway but also by FUN14 domain-containing 1 (FUNDC1) or Bcl2 interacting protein 3 (BNIP3) and BNIP3-like (BNIP3L/NIX) pathways. Several studies have shown that dysregulated mitophagy is involved in cardiac dysfunction induced by aging, aortic stenosis, myocardial infarction or diabetes. The cardioprotective role of mitophagy is well described, whereas excessive mitophagy could contribute to cell death and cardiac dysfunction. In this review, we summarize the mechanisms involved in the regulation of cardiac mitophagy and its role in physiological condition. We focused on cardiac mitophagy during and following myocardial infarction by highlighting the role and the regulation of PI NK1/parkin-; FUNDC1-; BNIP3- and BNIP3L/NIX-induced mitophagy during ischemia and reperfusion. Full article
(This article belongs to the Special Issue Mitophagy: From Molecular Mechanisms to Diseases)
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38 pages, 10178 KiB  
Review
Molecular Mechanisms and Regulation of Mammalian Mitophagy
by Vinay Choubey, Akbar Zeb and Allen Kaasik
Cells 2022, 11(1), 38; https://doi.org/10.3390/cells11010038 - 23 Dec 2021
Cited by 43 | Viewed by 6396
Abstract
Mitochondria in the cell are the center for energy production, essential biomolecule synthesis, and cell fate determination. Moreover, the mitochondrial functional versatility enables cells to adapt to the changes in cellular environment and various stresses. In the process of discharging its cellular duties, [...] Read more.
Mitochondria in the cell are the center for energy production, essential biomolecule synthesis, and cell fate determination. Moreover, the mitochondrial functional versatility enables cells to adapt to the changes in cellular environment and various stresses. In the process of discharging its cellular duties, mitochondria face multiple types of challenges, such as oxidative stress, protein-related challenges (import, folding, and degradation) and mitochondrial DNA damage. They mitigate all these challenges with robust quality control mechanisms which include antioxidant defenses, proteostasis systems (chaperones and proteases) and mitochondrial biogenesis. Failure of these quality control mechanisms leaves mitochondria as terminally damaged, which then have to be promptly cleared from the cells before they become a threat to cell survival. Such damaged mitochondria are degraded by a selective form of autophagy called mitophagy. Rigorous research in the field has identified multiple types of mitophagy processes based on targeting signals on damaged or superfluous mitochondria. In this review, we provide an in-depth overview of mammalian mitophagy and its importance in human health and diseases. We also attempted to highlight the future area of investigation in the field of mitophagy. Full article
(This article belongs to the Special Issue Mitophagy: From Molecular Mechanisms to Diseases)
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Graphical abstract

25 pages, 1613 KiB  
Review
Mitophagy: Molecular Mechanisms, New Concepts on Parkin Activation and the Emerging Role of AMPK/ULK1 Axis
by Roberto Iorio, Giuseppe Celenza and Sabrina Petricca
Cells 2022, 11(1), 30; https://doi.org/10.3390/cells11010030 - 23 Dec 2021
Cited by 75 | Viewed by 8792
Abstract
Mitochondria are multifunctional subcellular organelles essential for cellular energy homeostasis and apoptotic cell death. It is, therefore, crucial to maintain mitochondrial fitness. Mitophagy, the selective removal of dysfunctional mitochondria by autophagy, is critical for regulating mitochondrial quality control in many physiological processes, including [...] Read more.
Mitochondria are multifunctional subcellular organelles essential for cellular energy homeostasis and apoptotic cell death. It is, therefore, crucial to maintain mitochondrial fitness. Mitophagy, the selective removal of dysfunctional mitochondria by autophagy, is critical for regulating mitochondrial quality control in many physiological processes, including cell development and differentiation. On the other hand, both impaired and excessive mitophagy are involved in the pathogenesis of different ageing-associated diseases such as neurodegeneration, cancer, myocardial injury, liver disease, sarcopenia and diabetes. The best-characterized mitophagy pathway is the PTEN-induced putative kinase 1 (PINK1)/Parkin-dependent pathway. However, other Parkin-independent pathways are also reported to mediate the tethering of mitochondria to the autophagy apparatuses, directly activating mitophagy (mitophagy receptors and other E3 ligases). In addition, the existence of molecular mechanisms other than PINK1-mediated phosphorylation for Parkin activation was proposed. The adenosine5′-monophosphate (AMP)-activated protein kinase (AMPK) is emerging as a key player in mitochondrial metabolism and mitophagy. Beyond its involvement in mitochondrial fission and autophagosomal engulfment, its interplay with the PINK1–Parkin pathway is also reported. Here, we review the recent advances in elucidating the canonical molecular mechanisms and signaling pathways that regulate mitophagy, focusing on the early role and spatial specificity of the AMPK/ULK1 axis. Full article
(This article belongs to the Special Issue Mitophagy: From Molecular Mechanisms to Diseases)
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Graphical abstract

10 pages, 747 KiB  
Review
Mitophagy in Yeast: Molecular Mechanism and Regulation
by Aleksei Innokentev and Tomotake Kanki
Cells 2021, 10(12), 3569; https://doi.org/10.3390/cells10123569 - 17 Dec 2021
Cited by 14 | Viewed by 4086
Abstract
Mitophagy is a type of autophagy that selectively degrades mitochondria. Mitochondria, known as the “powerhouse of the cell”, supply the majority of the energy required by cells. During energy production, mitochondria produce reactive oxygen species (ROS) as byproducts. The ROS damage mitochondria, and [...] Read more.
Mitophagy is a type of autophagy that selectively degrades mitochondria. Mitochondria, known as the “powerhouse of the cell”, supply the majority of the energy required by cells. During energy production, mitochondria produce reactive oxygen species (ROS) as byproducts. The ROS damage mitochondria, and the damaged mitochondria further produce mitochondrial ROS. The increased mitochondrial ROS damage cellular components, including mitochondria themselves, and leads to diverse pathologies. Accordingly, it is crucial to eliminate excessive or damaged mitochondria to maintain mitochondrial homeostasis, in which mitophagy is believed to play a major role. Recently, the molecular mechanism and physiological role of mitophagy have been vigorously studied in yeast and mammalian cells. In yeast, Atg32 and Atg43, mitochondrial outer membrane proteins, were identified as mitophagy receptors in budding yeast and fission yeast, respectively. Here we summarize the molecular mechanisms of mitophagy in yeast, as revealed by the analysis of Atg32 and Atg43, and review recent progress in our understanding of mitophagy induction and regulation in yeast. Full article
(This article belongs to the Special Issue Mitophagy: From Molecular Mechanisms to Diseases)
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22 pages, 1863 KiB  
Review
Mitophagy in Yeast: Decades of Research
by Ingrid Bhatia-Kissova and Nadine Camougrand
Cells 2021, 10(12), 3541; https://doi.org/10.3390/cells10123541 - 15 Dec 2021
Cited by 5 | Viewed by 4842
Abstract
Mitophagy, the selective degradation of mitochondria by autophagy, is one of the most important mechanisms of mitochondrial quality control, and its proper functioning is essential for cellular homeostasis. In this review, we describe the most important milestones achieved during almost 2 decades of [...] Read more.
Mitophagy, the selective degradation of mitochondria by autophagy, is one of the most important mechanisms of mitochondrial quality control, and its proper functioning is essential for cellular homeostasis. In this review, we describe the most important milestones achieved during almost 2 decades of research on yeasts, which shed light on the molecular mechanisms, regulation, and role of the Atg32 receptor in this process. We analyze the role of ROS in mitophagy and discuss the physiological roles of mitophagy in unicellular organisms, such as yeast; these roles are very different from those in mammals. Additionally, we discuss some of the different tools available for studying mitophagy. Full article
(This article belongs to the Special Issue Mitophagy: From Molecular Mechanisms to Diseases)
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22 pages, 2773 KiB  
Review
Parkin beyond Parkinson’s Disease—A Functional Meaning of Parkin Downregulation in TDP-43 Proteinopathies
by Katarzyna Gaweda-Walerych, Emilia Jadwiga Sitek, Ewa Narożańska and Emanuele Buratti
Cells 2021, 10(12), 3389; https://doi.org/10.3390/cells10123389 - 01 Dec 2021
Cited by 8 | Viewed by 3041
Abstract
Parkin and PINK1 are key regulators of mitophagy, an autophagic pathway for selective elimination of dysfunctional mitochondria. To this date, parkin depletion has been associated with recessive early onset Parkinson’s disease (PD) caused by loss-of-function mutations in the PARK2 gene, while, in sporadic [...] Read more.
Parkin and PINK1 are key regulators of mitophagy, an autophagic pathway for selective elimination of dysfunctional mitochondria. To this date, parkin depletion has been associated with recessive early onset Parkinson’s disease (PD) caused by loss-of-function mutations in the PARK2 gene, while, in sporadic PD, the activity and abundance of this protein can be compromised by stress-related modifications. Intriguingly, research in recent years has shown that parkin depletion is not limited to PD but is also observed in other neurodegenerative diseases—especially those characterized by TDP-43 proteinopathies, such as amyotrophic lateral sclerosis (ALS) and frontotemporal lobar degeneration (FTLD). Here, we discuss the evidence of parkin downregulation in these disease phenotypes, its emerging connections with TDP-43, and its possible functional implications. Full article
(This article belongs to the Special Issue Mitophagy: From Molecular Mechanisms to Diseases)
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